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破骨细胞集落刺激因子和巨噬细胞集落刺激因子在破骨细胞发育过程中的相对作用。

Relative roles of osteoclast colony-stimulating factor and macrophage colony-stimulating factor in the course of osteoclast development.

作者信息

Lee T H, Fevold K L, Muguruma Y, Lottsfeldt J L, Lee M Y

机构信息

Department of Biological Structure, University of Washington School of Medicine, Seattle 98195.

出版信息

Exp Hematol. 1994 Jan;22(1):66-73.

PMID:8282061
Abstract

Although recent studies have shown that osteopetrotic (op/op) mice lack macrophage colony-stimulating factor (M-CSF or CSF-1), the precise role of M-CSF in the development of immature osteoclasts remains unknown. Using a recently discovered osteoclast-specific colony-stimulating factor (O-CSF) and in vitro long-term bone marrow culture systems, we investigated the ability of op/op and control marrow stromal cells to support the production of O-CSF-responsive clonogenic osteoclast progenitors (colony-forming unit-osteoclast [CFU-O]) from inoculated normal stem cells. Remarkably, op/op stromal cell cultures produced five times as many nonadherent cells as control cultures throughout the experimental period of 14 weeks; an average of 37% of these cells were nonviable compared with 8% in control cultures. Significantly higher numbers of CFU-O were found in op/op cultures than in control cultures; the CFU-O in op/op and control cultures were proliferating at a similar rate. Higher numbers of calcitonin receptor-bearing cells were found when harvested cells from op/op flasks were cultured with 1,25(OH)2D3. These studies clearly show that op/op marrow stromal cells can support the differentiation and proliferation of osteoclast progenitors from inoculated stem cells and provide the first experimental evidence that M-CSF is not essential for the early stages of osteoclast development. We hypothesize that while O-CSF supports proliferation of osteoclast progenitors, M-CSF plays a role in the later development and maturation of the progenitor as well as in the prevention of cell death.

摘要

尽管最近的研究表明,骨石化(op/op)小鼠缺乏巨噬细胞集落刺激因子(M-CSF或CSF-1),但M-CSF在未成熟破骨细胞发育中的精确作用仍然未知。利用最近发现的破骨细胞特异性集落刺激因子(O-CSF)和体外长期骨髓培养系统,我们研究了op/op和对照骨髓基质细胞支持从接种的正常干细胞产生O-CSF反应性克隆破骨细胞祖细胞(集落形成单位-破骨细胞[CFU-O])的能力。值得注意的是,在整个14周的实验期间,op/op基质细胞培养物产生的非贴壁细胞数量是对照培养物的五倍;这些细胞中平均37%不可存活,而对照培养物中为8%。在op/op培养物中发现的CFU-O数量显著高于对照培养物;op/op和对照培养物中的CFU-O以相似的速率增殖。当将来自op/op培养瓶的收获细胞与1,25(OH)2D3一起培养时,发现有更多的降钙素受体阳性细胞。这些研究清楚地表明,op/op骨髓基质细胞可以支持接种干细胞来源的破骨细胞祖细胞的分化和增殖,并提供了首个实验证据,即M-CSF对于破骨细胞发育的早期阶段并非必不可少。我们推测,虽然O-CSF支持破骨细胞祖细胞的增殖,但M-CSF在祖细胞的后期发育和成熟以及预防细胞死亡中发挥作用。

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